Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Peptide Library/ARA-290
Immune & Anti-Inflammatory
cibinetide · Helix B surface peptide · HBSP · pHBSP
An erythropoietin fragment that keeps EPO tissue-protective signalling and discards the blood-cell effect entirely — with genuine randomised human trial data in small-fibre neuropathy.
Erythropoietin does two unrelated things. It stimulates red blood cell production through the classical EPO receptor homodimer, and it protects injured tissue through a completely different receptor — the innate repair receptor, a heterodimer of the EPO receptor and CD131. The tissue-protective effect is what made EPO interesting in stroke and cardiac injury; the erythropoietic effect, with its thrombotic risk, is what made it unusable there.
ARA-290 is the answer to that problem: an 11-residue peptide from the helix B region of EPO that engages the innate repair receptor without touching the classical one. It has no erythropoietic activity at all, which removes the haematocrit and thrombosis concerns wholesale.[1]
It has real human trial data — randomised, placebo-controlled work in sarcoidosis- associated small-fibre neuropathy reporting improvements in corneal nerve fibre measures and in patient-reported neuropathic symptoms.[2] That places it well above most of this library, even though the trials are small and the compound remains unapproved.
Corneal confocal microscopy measures actual nerve fibre density. A compound showing improvement on that, in a randomised placebo-controlled design, is doing something considerably better evidenced than most of what sits alongside it in a research-peptide catalogue.
Innate repair receptor agonism. ARA-290 binds the EPOR/CD131 heterodimer expressed on injured tissue, immune cells and neurons. Signalling through this receptor is anti-inflammatory, anti-apoptotic and tissue-protective.
No classical EPO receptor activity. The peptide does not engage the receptor homodimer that drives erythropoiesis, so haemoglobin, haematocrit and thrombotic risk are unaffected. This is the design achievement.
Small nerve fibre effects. Reported regeneration of small nerve fibres and reduction of neuropathic pain signalling, which is where the clinical programme concentrated.
Immune modulation. Shifts macrophage phenotype toward resolution and reduces pro-inflammatory cytokine production.
Short half-life, sustained effect. Clearance is rapid, but reported clinical effects persist beyond exposure — consistent with a signal that initiates a repair programme rather than one requiring continuous receptor occupancy.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Randomised placebo-controlled trials reported improvements in corneal nerve fibre measures and in patient-reported neuropathic symptoms and pain in sarcoidosis-associated small-fibre neuropathy.
Confirmed across studies — no change in haemoglobin or haematocrit, which is the property distinguishing it from EPO and removing the thrombotic concern.
Reported protection in renal, cardiac, neurological and diabetic injury models via innate repair receptor signalling.
Clinical work has extended into diabetic neuropathy and metabolic endpoints, with reported effects on neuropathic symptoms.
Designations obtained for sarcoidosis and other rare indications — a development incentive rather than an approval.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Extrapolated from the sarcoidosis and diabetic neuropathy work to neuropathy generally. Reasonable and unproven outside the studied populations.
The community framing, extrapolated from pre-clinical tissue-protection models to healthy adults.
Proposed; not studied in these populations.
The theoretically attractive property — resolution signalling rather than suppression. Not demonstrated as a substitute for anything.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The dominant community report, typically over several weeks, and aligning with the population the trials studied.
Broadly reported and unmeasured.
Consistent with the clinical safety findings.
Reported, and consistent with a repair-initiating rather than occupancy-dependent mechanism.
Limits the anecdotal base considerably.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
No significant adverse-event signal reported in the clinical programme at studied doses and durations.
The absence of erythropoiesis removes the principal safety concern that attaches to EPO itself.
The studies ran weeks to months in defined patient populations. Long-term use in healthy adults is uncharacterised.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Tissue protection works by preventing cell death, which carries the standard theoretical concern about cells that should be dying.
Shifting macrophage phenotype persistently in someone without an inflammatory pathology has no characterisation.
ARA-290 is EPO-derived. Whether it interferes with anti-doping assays is not something an athlete should discover experimentally.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The main complaint.
Consistent with the trial data, and also with low usage volume.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The sarcoidosis small-fibre neuropathy trials used 4 mg once daily by subcutaneous injection over a defined course of weeks — a genuine trial-derived dose, which is rare in this library.
| Setting | Dose | Route | Duration |
|---|---|---|---|
| Sarcoidosis SFN trials | 4 mg daily | Subcutaneous | Weeks (trial-defined) |
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
A randomised trial established both a dose and a duration. Departing from it discards the one piece of real guidance available.
The trials ran defined courses, and the reported persistence of effect after stopping supports that structure.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Common community dosing, below the trial figure — usually on cost grounds rather than any pharmacological reasoning.
Used by those following the published protocol.
Typical community course length, roughly matching the trial durations.
| Approach | Dose | Frequency | Duration |
|---|---|---|---|
| Cost-limited | 1 – 2 mg | Daily | 4–8 weeks |
| Trial-matched | 4 mg | Daily | 4–8 weeks |
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
None.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Three different anti-inflammatory or repair mechanisms. Plausible grouping, no interaction data.
Mitochondrial dysfunction features in neuropathy pathophysiology, which makes the pairing conceptually reasonable and entirely untested.
An EPO-derived peptide in a tested athlete is a question to resolve before use, not after.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The typical stack context.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
4 mg daily subcutaneously over a defined course, with corneal confocal microscopy and validated symptom instruments as endpoints.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
A published dose, route and duration with objective endpoints is available. Very few compounds here offer that.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The general community pattern.
Neither documented protocol includes it.
ARA-290 has better human trial evidence than almost anything else in this library, in an indication most of its buyers have never heard of. It also has the most elegant design rationale here: it was built to keep the tissue-protective half of erythropoietin and discard the half that made erythropoietin dangerous.
ARA-290 is not approved anywhere, and its development programme appears to have stalled. It held FDA orphan drug designation for sarcoidosis-associated small fibre neuropathy, and reporting indicates the developer has wound down with no active US investigational new drug application and no phase 3 programme. If accurate, that means the best trial evidence in this library belongs to a compound nobody is currently developing — which is a comment on drug development economics in small indications rather than on the data. It has genuine randomised human trial data — small, in specific neuropathy populations — which places it above most of this library and well below an approved drug. It has not completed a confirmatory phase 3 programme, and it holds orphan designation rather than authorisation.
Pathophysiology
Erythropoietin does two separable things. Through the classical homodimeric EPO receptor it drives red cell production. Through a heteromeric receptor — EPO receptor paired with the beta-common receptor, sometimes called the innate repair receptor — it produces tissue protection and anti-inflammatory effects.
Mechanistic rationale
EPO looked promising in stroke and other tissue injury, and the trials disappointed — partly because raising haematocrit and thrombotic risk in already unwell patients is a poor trade. ARA-290 is an eleven-residue peptide derived from a region of EPO that engages the innate repair receptor without engaging the classical one. No rise in haematocrit, no thrombotic liability, tissue protection retained. Whether it delivers is a separate question; the design reasoning is the cleanest in this library.
Community reports
The distinction is rarely understood by people buying it, who frequently assume it is an EPO analogue in the performance sense. It is specifically engineered not to be, and it would be useless for that purpose.
Components carrying the argument: Innate repair receptor — EPOR/βcR heteromer
Pathophysiology
Small fibre neuropathy damages thinly myelinated and unmyelinated nerve fibres, producing burning pain, autonomic symptoms and impaired thermal sensation. It is common in sarcoidosis and there is little that treats it.
Mechanistic rationale
Randomised controlled trials in this population reported improvements in corneal nerve fibre measures and in symptom and quality-of-life scores. Corneal confocal microscopy is an objective structural endpoint, not a questionnaire — which makes this among the better-designed studies of any compound in this library. The trials were small and the programme has not been completed.
Community reports
Almost nobody using this compound has sarcoidosis, which is a striking mismatch between where the evidence is and where the use is.
Components carrying the argument: Innate repair receptor, small fibre protection
Pathophysiology
Diabetic neuropathy involves metabolic and microvascular injury to small fibres, and it is the leading cause of non-traumatic amputation through the loss of protective sensation.
Mechanistic rationale
ARA-290 has been studied in type 2 diabetes with neuropathy, with reported improvements in corneal nerve fibre measures and symptom scores. The mechanism transfers straightforwardly from the sarcoidosis work. Glycaemic control remains the only intervention shown to alter the course of diabetic neuropathy — everything else, including this, treats symptoms or nerve structure without addressing the driver.
Community reports
The most common reason for community use, generally in people with diabetic or idiopathic neuropathy who have exhausted the usual options.
Components carrying the argument: Small fibre protection and repair
Pathophysiology
Neuropathic pain arises from damage to the somatosensory system itself and responds poorly to conventional analgesics.
Mechanistic rationale
Pain scores improved in the neuropathy trials, which is a real finding within those populations. Extending it to chronic pain generally — including fibromyalgia and chronic pelvic pain, where it is sometimes discussed — goes beyond what was studied, and fibromyalgia in particular is a central sensitisation disorder rather than a small fibre one, though the two do co-occur.
Community reports
Used across a wider range of pain conditions than the evidence covers.
Components carrying the argument: Nerve fibre protection; central effects unestablished
Pathophysiology
Platinum agents and taxanes damage peripheral nerves, and the resulting neuropathy is dose-limiting, frequently permanent, and has no established preventive treatment.
Mechanistic rationale
This is mechanistically the most natural extension of the small fibre work and one of the largest unmet needs in supportive oncology. It has not been tested. Anyone in cancer treatment should raise this with their oncology team — tissue-protective agents given alongside chemotherapy carry a theoretical concern about protecting the tumour as well as the nerve.
Community reports
Occasionally used in this context, generally without the oncologist knowing.
Components carrying the argument: Tissue protection
Pathophysiology
Ischaemia-reperfusion injury shares a common pathway across organs: inflammatory activation, oxidative stress and apoptosis in tissue that has been transiently deprived of perfusion.
Mechanistic rationale
The innate repair receptor is expressed widely, so animal work spans kidney, heart, retina, spinal cord and central nervous tissue. That breadth is a mechanistic argument rather than a clinical one, and a compound with an effect everywhere in animals frequently has one nowhere in people — which is precisely what happened to erythropoietin itself.
Community reports
Cited in longevity and general tissue-protection contexts on the strength of the preclinical breadth.
Components carrying the argument: Innate repair receptor, expressed broadly
| Condition | Evidence | Endpoint | The thing to know |
|---|---|---|---|
| Sarcoidosis small fibre neuropathy | Randomised human | Corneal nerve fibres + symptoms | Objective structural endpoint |
| Diabetic neuropathy | Human, smaller | Nerve fibres + symptoms | Glycaemic control is the disease-modifier |
| Neuropathic pain | Within those trials | Pain scores | Extension beyond them is inference |
| Chemo-induced neuropathy | None | — | Natural extension; raise with oncology |
| Organ / ischaemia protection | Animal, broad | — | EPO looked the same and failed in trials |
| Haematocrit effect | None by design | — | Not an EPO analogue in the performance sense |
For diabetic neuropathy: glycaemic control is the only intervention shown to change the disease course. For the pain: duloxetine, pregabalin, gabapentin, amitriptyline and topical capsaicin. Foot care and annual screening prevent the outcome that actually costs people limbs. Address vitamin B12 deficiency, alcohol and thyroid disease before assuming a diabetic cause — all three are common, all three are treatable, and all three present identically.
For sarcoidosis: corticosteroids and steroid-sparing immunosuppression for the underlying disease, managed by a specialist. Small fibre neuropathy in this population is genuinely poorly served, which is why the trials were run there.
For neuropathic pain generally: the same drug classes above, plus multidisciplinary pain management, which outperforms any single agent in chronic pain of any cause.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Supplied lyophilised, commonly 10 mg per vial. At the 4 mg trial dose a 10 mg vial is only two and a half days, which makes trial-matched dosing expensive.
Lyophilised: −20 °C. Reconstituted: 2–8 °C.
Commonly 10 mg lyophilised vials.
An 11-residue peptide with ordinary handling requirements.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved anywhere. ARA-290 (cibinetide) has completed randomised clinical trials and holds orphan drug designations for rare indications, but has no marketing approval. Supplied as a research chemical.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: orphan designation; developer wind-down and absence of an active IND. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
ARA-290 is derived from erythropoietin. Although it lacks erythropoietic activity, EPO and its derivatives are covered by WADA S2, and an athlete should assume prohibition and verify before use.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
